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Impact of smoking on platelet function of ticagrelor versus clopidogrel in minor stroke or transient ischaemic attack

First author：Yang Yingying

Corresponding author：Wang Yilong,Pan Yuesong

clopidogrel smoking stroke ticagrelor transient ischaemic attack transient ischaemic stroke. dual antiplatelet therapy platelet reactivity;

essential_information

  • Person in charge：Yang Yingying
  • Data Sources： PRINCE
  • Number of papers：PRINCE20200227
  • Published time：2020-05-10

2020-05-10

Published articles

Journal：European Journal of Neurology

Publication type: Original Contributions

IF(IF): 6.089

PMID: 32052517 Link To Pubmed Full text Download

Background And Purpose

It remains unclear whether smoking status has an impact on platelet reactivity and clinical outcomes of ticagrelor versus clopidogrel in patients with acute minor stroke or transient ischaemic attack (TIA).

Method

A subgroup analysis of a randomized controlled trial was conducted. Patients with minor stroke or TIA were randomized for treatment with ticagrelor plus aspirin or clopidogrel plus aspirin. Platelet reactivity was assessed by VerifyNow P2Y12 assay at baseline, 7 + 2 days and 90 ± 7 days. High on-treatment platelet reactivity (HOPR) was defined as P2Y12 reaction units >208. Clinical outcomes included any stroke, composite clinical vascular events and bleeding events at 90 days. Patients who smoked one or more cigarettes per day for at least 1 year in their lives were defined as smokers.

Conclusion

Among patients with minor stroke or TIA, ticagrelor was superior to clopidogrel in inhibiting platelet reactivity and reducing the risk of new stroke, particularly for non-smokers.

Main results

Of 675 patients enrolled in the trial, 370 patients (54.8%) were smokers. At 7 + 2 days, the proportion of HOPR in ticagrelor versus clopidogrel was significantly lower in smokers (5.2% vs. 21.8%) and non-smokers (2.3% vs. 34.4%). There were marginal significant interactions between treatment groups and smoking status for the proportion of HOPR (P = 0.058). At 90 ± 7 days, there were significant interactions between treatment groups and smoking status for the risk of new stroke (smokers: 7.0% vs. 4.9%; hazard ratio, 1.57; 95% confidence interval, 0.65-3.79; P = 0.39; non-smokers: 5.3% vs. 13.5%; hazard ratio, 0.39; 95% confidence interval, 0.17-0.91; P = 0.01; P for interaction = 0.02).